anti- BNIP3L antibody

Este producto es parte de BNIP3 - BCL2 interacting protein 3 (Like)
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935106861
info@markelab.com
name
anti- BNIP3L antibody
category
Primary Antibodies
provider
FineTest
reference
FNab00929
tested applications
ELISA, WB, IHC

Description

This gene encodes a protein that belongs to the pro-apoptotic subfamily within the Bcl-2 family of proteins. The encoded protein binds to Bcl-2 and possesses the BH3 domain. The protein directly targets mitochondria and causes apoptotic changes, including loss of membrane potential and the release of cytochrome c.

Documents del producto

Instrucciones
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Data sheet

Product specifications

Category
Primary Antibodies
Immunogen Target
BCL2/adenovirus E1B 19kDa interacting protein 3-like
Host
Rabbit
Reactivity
human,mouse,rat
Recommended Dilution
WB: 1:500 - 1:2000; IHC: 1:50 - 1:200
Clonality
polyclonal
Conjugation
Unconjugated
Isotype
IgG
Observed MW
30 kDa, 45 kDa
Purity
≥95% as determined by SDS-PAGE
Purification
Immunogen affinity purified
Size 1
100µg
Form
liquid
Tested Applications
ELISA, WB, IHC
Storage
PBS with 0.02% sodium azide and 50% glycerol pH 7.3 , -20℃ for 12 months (Avoid repeated freeze / thaw cycles.)
UniProt ID
O60238
Gene ID
665
Alias
BNIP3L,BNIP3A,BNIP3H,NIX,Adenovirus E1B19K-binding protein B5,BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like
Background
Antibody anti-BNIP3L
Status
RUO
Note
This product is for research use only.

Descripción

BCL2 Interacting Protein 3 Like (BNIP3L), also known as NIX, is a member of the BCL2 family of proteins and plays a critical role in programmed cell death and mitochondrial quality control. BNIP3L is known to interact with BCL2 and other apoptotic regulators, promoting mitochondrial autophagy (mitophagy), a selective process that removes damaged or dysfunctional mitochondria to maintain cellular homeostasis. Its function is particularly crucial under conditions of hypoxia, where BNIP3L is upregulated, contributing to cell survival by mitigating oxidative stress and preventing the accumulation of damaged mitochondria. In the context of erythroid maturation, BNIP3L is essential for mitophagy-mediated clearance of mitochondria, a necessary step in the development of red blood cells. Dysregulation of BNIP3L has been implicated in various pathologies, including cancer, where its role can vary between promoting cell death in some contexts and contributing to tumor survival and resistance in others. Additionally, alterations in BNIP3L function are associated with neurodegenerative diseases due to impaired mitochondrial dynamics and clearance. This duality highlights the importance of BNIP3L as a potential therapeutic target for addressing diseases linked to apoptosis and mitochondrial dysfunction.

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